The main objective of this research is to determine if there is an interaction between drugs which cause changes in drug metabolism and the potential of inhaled chlorinated hydrocarbons to produce either spontaneous or epinephrine-induced cardiac arrhythmias. Agents known to alter drug metabolism, e.g. phenobarbital and SKF 525-A, will be administered to rabbits. Control and treated animals will then be exposed in a dynamic inhalation chamber to chloroform, metylchloroform, trichloroethylene, tetrachloroethylene or halothane. Lead II ECG recordings will be made to determine if the drug pretreatment alters the capacity of these compounds for producing arrhythmias. This will be assessed by comparison of the threshold concentrations of the halogenated hydrocarbons which produce arrhythmias, both spontaneous and epinephrine-induced, in the control and treated groups as well as by measurement of the amount of epinephrine needed to produce such an effect at a fixed concentration of halogenated hydrocarbon. In cases where such interactions are found, attempts will be made to verify the cause and effect relationship between alteration of drug metabolism and arrhythmigenic potential by measurement of the blood levels of the parent compound and its metabolites at the time and conditions of such an interaction. Such studies will help to determine if individuals with altered hepatic functions might be more susceptible to the arrhythmigenic affects of halogenated hydrocarbons commonly encountered in occupational situations or anesthesia.